A synapse is the structure through which neurons communicate by the release of neurotransmitters. The presynaptic terminal is at the end of cell extensions known as axons that transmit electrical signals in the neuron system. In addition, the presynaptic terminal has an assortment of proteins synthesized in the cell body and are transported down the axons to aid in the fusion of the vesicles with the cell membrane to release their contents. Before communication can occur, a developing neuron must extend an axon, synthesize synaptic proteins, and transport them to synaptic terminals. Many proteins that play a role in synaptic function have been identified. Evidence suggests that some synaptic proteins may contribute to neurite outgrowth as well.

One of the essential proteins involved in the these processes is synaptotagmin(syt). Syt is the calcium sensor in which triggers the membrane fusion event. In a previous study, it was observed that an increased production of syt in neurons correlated with increased axon branching. It has also been noted that syt is present at the earliest stages of axon development. These observations suggest that syt may be a contributing factor in developing axon outgrowth and branching. We study axon branching using neurons from the superior cervical ganglion (SCG) of neonatal rats. These neurons will be infected in vitro using a virus to cause an overproduction of syt that is fused to YFP. YFP is a fluorescent tag that will act as a surrogate visual marker for the presence of syt. To control for non-specific viral effects, YFP alone will be introduced via the same method. The parallel experiments are expected to reveal increased axon branching in the syt-YFP infected cells relative to the cells infected with YFP alone. The results of the experiment will be observed using confocal microscopy and live cell imaging.